English: (a) Schematic figure of early-somite stage embryo and Wnt/β-catenin-mediated endoderm patterning. Wnts (oncogene), secreted from the mesoderm (red), signal to the adjacent posterior endoderm (blue) to repress foregut development by activating the homeodomain repressor vent2, which in turn inhibits the expression of key foregut genes such as hhex (hematopoietically expressed homeobox, transcription factor) and foxa2 (forkhead box A2, transcription factor) in the posterior endoderm. The anterior endoderm (green) secretes a number of Wnt-antagonists that block the Wnt signals from the mesoderm, allowing hhex and foxa2 expression to impart foregut identity. The hhex-expressing anterior endoderm then sends a signal to the adjacent mesoderm inducing it to become cardiac. Later in development, the cardiogenic mesoderm signals back FGF (fibroblast growth factor) to the anterior endoderm, inducing a subset of the foregut endoderm to adopt a hepatic fate. (b) Lateral view of an embryo (e8.25) (2–4 somite stage). At this stage the definitive endoderm (DE) is forming a foregut pocket. The liver is induced by FGF signals from the cardiogenic mesoderm and BMPs (bone morphogenetic protein) from the septum transversum mesenchyme (STM). Foregut endoderm isolated after the 5–7 somite stage will express liver genes such as albumin, indicating that hepatic fate is specified. Different doses of FGF appear to induce lung and ventral pancreas from the foregut progenitors. Signals from the dorsal mesoderm (Wnt ligands) repress hepatic fate in the dorsal endoderm.

English: Endoderm patterning and foregut development